Evidence map›Paper›PMID 25768401›Full record

Trial reportBlood cancer journal2015

Evaluation of plitidepsin in patients with primary myelofibrosis and post polycythemia vera/essential thrombocythemia myelofibrosis: results of preclinical studies and a phase II clinical trial.

A Pardanani, A Tefferi, P Guglielmelli, C Bogani, N Bartalucci, J Rodríguez, S Extremera, I Pérez, V Alfaro, A M Vannucchi

Open access · goldAbstract readClinical Trial, Phase II
In one paragraph

Trial report in Blood cancer journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Plitidepsin: design, development, and potential place in therapy.Drug design, development and therapy · 2017
    Review
  4. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

A PardananiDivision of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA.
A TefferiDivision of Hematology, Department of Medicine, Mayo Clinic, Rochester, MN, USA.
P GuglielmelliDepartment of Experimental and Clinical Medicine, University of Florence, Careggi, Firenze, Italy.
C BoganiDepartment of Experimental and Clinical Medicine, University of Florence, Careggi, Firenze, Italy.
N BartalucciDepartment of Experimental and Clinical Medicine, University of Florence, Careggi, Firenze, Italy.
J RodríguezPharmaMar, Clinical R&D Department, Colmenar Viejo, Madrid, Spain.
S ExtremeraPharmaMar, Clinical R&D Department, Colmenar Viejo, Madrid, Spain.
I PérezPharmaMar, Clinical R&D Department, Colmenar Viejo, Madrid, Spain.
V AlfaroPharmaMar, Clinical R&D Department, Colmenar Viejo, Madrid, Spain.
A M VannucchiDepartment of Experimental and Clinical Medicine, University of Florence, Careggi, Firenze, Italy.
PharmaMar (Spain) · ESUniversity of Florence · ITMayo Clinic · USMayo Clinic in Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous data established that plitidepsin, a cyclic depsipeptide, exerted activity in a mouse model of myelofibrosis (MF). New preclinical experiments reported herein found that low nanomolar plitidepsin concentrations potently inhibited the proliferation of JAK2V617F-mutated cell lines and reduced colony formation by CD34+ cells of individuals with MF, at least in part through modulation of p27 levels. Cells of MF patients had significantly reduced p27 content, that were modestly increased upon plitidepsin exposure. On these premise, an exploratory phase II trial evaluated plitidepsin 5 mg/m(2) 3-h intravenous infusion administered on days 1 and 15 every 4 weeks (q4wk). Response rate (RR) according to the International Working Group for Myelofibrosis Research and Treatment consensus criteria was 9.1% (95% CI, 0.2-41.3%) in 11 evaluable patients during the first trial stage. The single responder achieved a red cell transfusion independence and stable disease was reported in nine additional patients (81.8%). Eight patients underwent a short-lasting improvement of splenomegaly. In conclusion, plitidepsin 5 mg/m(2) 3-h infusion q4wk was well tolerated but had a modest activity in patients with primary, post-polycythaemia vera or post-essential thrombocythaemia MF. Therefore, this trial was prematurely terminated and we concluded that further clinical trials with plitidepsin as single agent in MF are not warranted.

Indexed as

AgedCell ProliferationDepsipeptidesFemaleHumansJanus Kinase 2MaleMiddle AgedPeptides, CyclicPolycythemia VeraPrimary MyelofibrosisSplenomegalyThrombocythemia, EssentialDepsipeptidesJAK2 protein, humanJanus Kinase 2Peptides, Cyclicplitidepsin

Identifiers

PMID25768401
PMCPMC4382667
OpenAlexW1997871580

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.